Alzheimer's disease (also described as AD hereafter) is one of the most typical neurodegenerative diseases involving the old ages. Progressive memory defect or decline in spatial or linguistic cognitive function is main feature of this disease. It is understood that main cause of the decline in these cognitive function is amyloid beta peptides (also described as Aβhereafter) accumulate on cerebral parenchyma and then formed amyloid plaque causes degeneration of nerve cells (Non-patent document 2 and 3).
The accumulation of Aβ, consisting of especially 39-43 base length of amino acid, is considered the cause of AD (Non-patent document 1). Aβ is generated from amyloid precursor protein (also described as APP hereafter) by being cleaved with two kind of proteases, (β-secretase (also described as BACE1 hereafter) and γ-secretase, which are β-amyloid protease.
It is recently reported that the activity of BACE1 rises in the brain of AD patient and cerebral fluid (Non-patent document 4 and 5). This indicates that BACE1 is promising target for anti-AD medicine and is potential marker for AD.
In addition, generation of soluble APPβ (soluble Amyloid Precursor Protein also described as sAPP β (hereafter) relates to BACE1 activity and therefore has been used as indicator for screening for anti-AD medicine. Furthermore, it is reported that sAPP β is useful for marker for Alzheimer's disease (Non-patent document 6). Therefore, a method for quantifying sAPP β with accuracy and a high sensitivity is desired.